TOP A

******************************************************************************************************

15 April 2010)– From April 2011, European legislation (EC Directive 2004/24/EC) which has already been passed in 2004 will come into force which will effectively mean that ALL Herbal medicines will disappear from the shelves in our High Streets or internet shops within the EU. Freedom of choice in medicine is being taken away. You will only have access to treatments which are Pharmaceutical Drugs based in order to treat your own and your families ailments. No Chinese herbs, No Ayurvedic (Indian) herbs, No Western herbs, NO MEDICINAL HERBS WHATSOEVER. Chinese medicine practitioners will lose access to the majority of the herbs and medicines on which they rely. Consumers will NOT be able to buy any Chinese herbal products within the EU.--This legislation has been heavily influenced by the pharmaceutical industry, who want to protect their profit and will stand to gain by this legislation. There is not any evidence to prove that herbal medicine present a significant risk to the public under previous and present legislation, when policed properly.---“In the case of something like Chinese medicine, the safety issue is a red herring because hundreds of millions of people safely use Chinese medicine already and incredible amounts of research, safety data, usage data, and AER data is available in Asian countries if the EU officials cared to look into it. A blanket ban on products that have been safely used by billions of people for centuries seems to fly in the face of the modern vision of a harmonious, globally integrated society. “---“Getting a classical herbal medicine from a non-European traditional medicinal culture through the EU registration scheme is akin to putting a square peg into a round hole. The regulatory regime ignores and thus has not been adapted to the specific traditions. Such adaptation is required urgently if the directive is not to discriminate against non-European cultures and consequently violate human rights.”--Despite the petitions and demonstrations from herbal practitioners and consumers, as in April 2010, the UK government is showing clear intention to enforce this ban. Although there is still around 11 months away, some of our suppliers have already taken precautions to stop importing stocks in order to accommodate for this change in law and therefore, we are also reducing the stock level and stop stocking low demand products. We are expecting the shortage of supply on certain herbal products in coming months, as the UK based suppliers are calculating the risk of importing and stocking herbal products as the deadline of ban is looming. We advise our customers to consider stocking up on any medications which you are particularly reliant on, as there is a great chance that they will no longer be available in the UK from next year. Please raise the issue to your local MP and sign the petition here <http://www.gopetition.com/petitions/support-herbal-medicine.html> .

Herbal drug crackdown: Millions face having to buy remedies on black market as Europe tightens the rules

Patients could lose access to safe herbal medicines under EU rules, it was claimed yesterday. --Instead they could end up buying potentially dangerous supplies from the black market, say herbalists. --Sales of all herbal remedies, except for a small number of products for 'mild' illness, will be banned to the public under the new law to come in in 2011. -----At least six million Britons have consulted a herbal practitioner in the past two years, says research---Almost 2,500 UK qualified herbalists and Chinese medicine practitioners will also lose the right to supply a wide range of herbal medicines, because they are not signed up to a statutory regulation scheme. ---Unlike healthcare professionals, there is no regulation of herbalists. --The Government has launched a consultation on whether to bring in statutory regulation - which herbalists support. However, many fear the consultation process is too complicated, which could affect the chances of its success. --At least six million Britons have consulted a herbal practitioner in the past two years, according to research. --Leading medical herbalist Dr Ann Walker said: 'At present patients have access to top quality herbal products that are manufactured only for professional use, but we won't be allowed to supply them. --'Traditional remedies from China and India will only be available through the internet or backstreet suppliers, which could pose a serious health risk to the public.' --Dr Michael Dixon, of the Prince's Foundation for Integrated Health, said: 'We fear if the Government refuses statutory regulation, we will see a black market in herbal products, with unlicensed, potentially dangerous remedies[U1].' Some of these 'backstreet' medicines have been found to contain toxic heavy metals. Dr Dixon said statutory regulation was 'essential' but the public consultation closes on November 2. The Department of Health said there was no timeline for further action on a regulation scheme. ----And will this affect just the UK? Apparently not; it will be all of the EU. And the same effort is apparently also underway to essentially do the same in the US -- i.e., to rip away from the people of this planet the right and the ability to access and to use nutritional &herbal & other such traditionally effective and time-proven means of supporting and strengthening their own immune-systems and their own health. There is even, now, a legislative push in the US Congress to approve a piece of legislation that, if it passes into law, will greatly increase the control -- and the power -- and the industry-share -- of "Big Agriculture", at the expense of the small farmer and even, reportedly, say critics, at the expense of the average American, such that he or she will not be legally permitted to even grow a few edibles in the backyard garden. Should this happen, say critics, the consequence will also be that the availability of unadulterated, natural, foods will plummet.

***************************************************************************************************

Lycopene-rich tomato paste helps skin from within

Daily consumption of a lycopene-rich tomato paste reduced reddening of the skin after exposure to UV light, says a new study that supports the skin health potential of lycopene. --The tomato paste, giving a daily lycopene dose of 16 milligrams, was also found to reduce damage to mitochondrial DNA, a measure identified as a reliable marker of UV-ray exposure, according to findings published in British Journal of Dermatology. --“This study supports previous epidemiological, animal and human data reporting protective effects of lycopene and indicates that this agent also protects against UVR-induced tissue damage,” wrote researchers from the University of Manchester and Salford Royal NHS Foundation Trust, and Newcastle University. ---“Nutritional photoprotection with tomato products is a promising area for research, and further investigative and clinical studies are required to explore these novel findings,” they added. ---As an antioxidant, lycopene has been shown to have heart, blood pressure, prostate, osteoporosis, skin and other benefits in both natural and synthetic form and it has been commonly used in food supplements and nutricosmetic applications. -Study details --Twenty healthy women with an average age of 33 and skin types defined as phototype I/II were recruited to participate in the study. The women were randomly assigned to receive either 55 grams of tomato paste in olive oil, or just olive oil every day for 12 weeks. --Of the 17 women who completed the study, skin samples taken from the buttocks before and after 12 weeks of intervention showed that, while there were no changes in the control group, the dose of UV needed to cause reddening increased from 26.4 mJ/cm2 at the start to 36.6 mJ/cm2 after lycopene supplementation, a result which shows the improved resistance of the skin to reddening. ---Furthermore, lycopene supplementation was associated with a reduction in the UVA-induction of the matrix metalloprotease enzyme MMP-1, which plays a key role in degradation of the extracellular matrix during premature skin aging. “We anticipate that a range of commonly consumed foods containing highly processed tomato, could have similar effects if ingested in equivalent amounts, but this requires confirmation in further studies. Our data identifies lycopene-rich tomato paste to have properties appropriate for its potential development in systemic photoprotection,” stated the researchers. --Source: British Journal of Dermatology Published online ahead of print, doi: 10.1111/j.1365-2133.2010.10057.x “Tomato paste rich in lycopene protects against cutaneous photodamage in humans in vivo” Authors: M. Rizwan, I. Rodriguez-Blanco, A. Harbottle, M.A. Birch-Machin, R.E.B. Watson and L.E. Rhodes

****************************************************************************************************

Recipe for Tomato Paste—either buy a jar of tomato paste ( usually found in the grocery store in a middle eastern market and sometimes an Italian market—and mix with an olive oil and add the spice paprika and safflower and tumeric and black pepper mix well in olive oil and heat in pan til warm and let stay warm for 5 minutes –constantly stirring the mix as not to burn this—when done allow to cool –you can spoon this in –you can add it a side dish and use like a ketchup with out the sugar or HFCS—mix it in a tomato soup—add it to eggs

This will increase not only the lycopene content but other antioxidants as well—and you get the benefit of the anti cancer properties from these herbs—and you produce an anti aging remedy as well

******************************************************************************************************

“Fingers crossed” for article 13.5 acai antioxidants dossier

German fruit extract supplier TropExtract GMBH has submitted an article 13.5 proprietary and emerging science dossier linking Amazonian superfruit extract acai and antioxidant activity to the European Union health claims process. -- Sonja Hoffelner, TropExtract’s master of science nutrition said the company was being realistic about its prospects of success, especially given a limited number of trials in the dossier, and EFSA’s position that antioxidant activity is not necessarily beneficial in the body. --“There are some human intervention trials in our dossier, but only with disappointing results,” [U2]she said. “But there is evidence that an increased dietary intake of antioxidants from fruits are associated with reduced risks of a range of disease, including for example cancer. These results may not prove causality but they do indicate that we should not turn our backs on these compounds.” --She said the company was in dialogue with EFSA about the application. --“According to EFSA’s opinion that there is no evidence provided to establish that having antioxidant activity is a beneficial physiological effect[U3] we will have to cross our fingers,” Hoffelner said. ---“But we are speaking with them. Our next step is to specify the substance, which has a beneficial effect on the body. It’s an opportunity to move antioxidants forward.” ---TopExtract was planning an in vivo trial that could add to the weight of evidence. --Not sufficient to predict the occurrence of an effect --Earlier this year, EFSA’s Panel on Dietetic Products, Nutrition and Allergies (NDA issued negative opinions relating to 169 dossiers that included blackcurrant juice; royal jelly; acerola; guava; various grape juices and extracts; honey; olive and olive extracts; hibiscus; chorella algae; green tea; cranberry; lingonberry; sea buckthorn oil; prunes, bananas, resveratrol; pomegranate and pine bark extract. ---Other nutrients given the thumbs down included spirulina; triphala; chlorophyll; sulphoraphane glucosinolate; elderberry juice; glutathion; aged garlic; rooibos; ginseng; ginkgo biloba; cherries; echinacea ; bilberry ; curcumin and capsicum[U4]. --In its opinion the NDA stated that: “…no evidence has been provided to establish that having antioxidant activity/content and/or antioxidant properties is a beneficial physiological effect.” --It said it assumed those properties were to, “scavenge free radicals and/or to their reducing capacity.” --On the matter of protecting DNA, proteins and lipids from oxidative damage which were also claimed in the submissions, the NDA noted the absence of human studies using reliable risk factors or biomarkers. ---“The evidence provided in the animal and in vitro studies submitted is not sufficient to predict the occurrence of an effect of the food(s)/food constituent(s) on the protection of body cells and molecules such as DNA, proteins and lipids from oxidative damage in vivo in humans,” the NDA said--

GMOs in China

China is currently the sixth largest producer of genetically modified (GM) crops (3.8 million hectares in 2008, behind the United States, Argentina, Brazil, India, and Canada [1]. The Chinese government has granted safety certificates for commercial production of four biotech food and fibre crops, including insect resistant cotton, virus resistant papaya, virus resistant sweet pepper, and delayed ripening tomato. Transgenic plants like poplar and petunia are also approved for production. Among the hundreds of biotech products under development that have been approved for productive testing are insect resistant rice (Bt63), bacterial blight resistant rice (Xa21), high phytase corn, and high oil content canola. Other major crops undergoing field trials include insect resistant corn, high lysine content corn, wheat resistant to pre-harvest germination, and insect resistant soybeans. [U5] The regulatory approval of Chinese crops differs significantly from the regulatory approval processes in North America. In one major area alone, in China GM crops are approved by variety in contrast to regulation in North America where crops are regulated by GM event, as ISIS has insisted [2] (see Biosafety Alert, ISIS report). In North America the GM event, once approved in a variety can be bred into other varieties or land races without further regulatory approval [1]. The Chinese approach on regulating GM food crops is slower and apparently more reliable than regulatory approval in North America. Approval by variety may leave a dangerous loophole if the ‘variety’ actually includes more than one GM event, as it is in the unreliable, unpredictable nature of genetic modification that each event is unique and differs according as to where and in what form the GM insert has landed, and what kind of collateral damage has been done to the host genome (see [3] FAQ on Genetic Engineering, ISIS Tutorial). There is limited private sector research and development in agricultural biotechnology in China [1]. Biotech seed development in China is conducted by public research institutes and universities funded by various parts of the Chinese government, though marketing is often done by affiliated private companies. Foreign investment on research and production of biotech plants, livestock, and aquatic products is prohibited; but it is allowed in conventional seed production. China has approved four biotech crops/products for import as processing materials (soybeans, maize , canola, and cotton). The first batch of safety certificates was granted to imported biotech crops in 2004. The 28 varieties approved for import processing include the following traits: 15 herbicide tolerant, 3 reduced formation of undesirable fatty acids, 5 insect resistant, and 5 insect resistant and herbicide tolerace. Production of seeds for crops that are not genetically modified can be undertaken in partnership with multinational seed producers; but multinational corporation ownership is limited to minority shareholders in joint ventures with Chinese companies.

******************************************************************************************************

[U1]What Fear Mongering--always think in the worse these journalist would have you believe---the better stuff will come thorgh the back streets and the mainstream stuff will all be diluted anyway---soooo who is fearing--MainStream

[U2]The concept of Acai berry having some claims in some effect brings down on it the actually benefit---it is a good berry with antioxidants but the claims on mass reduction if they are legitimate never panned out --so again when you see some of the claims some of the marketing people do with these products you have to be aware that alot of it is hyperboleAcai berry has about the same antioxidant capacity as cherry's in the USA and the reason for the expense of the berry is due to the fact it is a light covered seed with a papper thin berry so you need alot to get anything out of them

[U3]Again here is a Problem--based on a drug Company running the directives on a nutraceutical as opposed to a pharmaseutical you are going to have this Kind of inaccuracy---the drug comanies for over 50-60 years have lambasted Vitamin C and yet there are 10's of thousands reesarch reports showing the validity of vitamin C at medium to high dose with any issue--And yet instititions like this run by the FDA will cause this kind of ignorance to thrive and cause people to doubt and be swayed by this type of Misinformation

[U4]Irony is that all of these things do impact benefit to health and longevity--- This works agains the EUGENICS PROGRAM being ENACTED-- So anything that has Life Extending Properties will be challenged with these Article 13---this is what Scientific America published that the FDA should adopt this type of stupidity---well it is the FDA through the efsa that is regulating Europe so the usa and canada ( not having much of an industry thanks to the gov't) will follow suit

[U5]China is following the trend of the west and that is Demociding there own people--years ago this would not have happened and today they are following the same dictates of the Monetary system --profit over value--the fact they have released GMO's at all shows a chink in the Chinese system is there and is being exploited as well---the very fact that they have not allowed foreign research in to assist is telling you that this is all gov't approved Eugenics--sad to say but in today's times there is nothing of value with anyone who reaches developmental stages of a 1st world caliber-

ScienceDaily (Feb. 8, 2009) — A new study makes important new findings on the role of hormone use on the risk of breast cancer, confirming that the use of estrogen plus progesterone increases the risk of both ductal and lobular breast cancer far more than estrogen-only; suggesting a two-year "safe" period for the use of estrogen and progesterone; and finding that the increased risk for ductal cancers observed in long-term past users of hormone replacement therapy drops off substantially two years after hormone use is stopped.--Previous studies have shown that hormone replacement therapy after menopause increases the risk of breast cancer and that use of a regimen that includes both estrogen and progesterone is more detrimental for the breast than the use of estrogen alone. But more data from large prospective studies are needed to fully characterize the impact of exogenous hormones (Exogenousor exogeneous) refers to an action or object coming from outside a system. It is the opposite of endogenous, something generated from within the system ) on breast cancer incidence by type of hormone preparation and histology of the cancer.---To investigate the association in more detail, American Cancer Society epidemiologists led by Eugenia E. Calle, PhD, did a prospective study of 68,369 postmenopausal women who were cancer-free at baseline in 1992. They examined the use of estrogen-only and estrogen and progesterone in current and former users of varying duration, and the subsequent risk of developing invasive ductal and lobular carcinoma of the breast. They also looked at whether the risk for each type of breast cancer and each type of hormone regimen varied by body mass index (BMI), stage of disease at diagnosis, and estrogen receptor (ER) and progesterone receptor (PR) status. For the present study, the follow-up period ended on June 30, 2005.---They confirmed the findings from previous work that estrogen and progesterone increases the risk of both ductal and lobular breast cancer far more estrogen alone. They also found the risk associated with use of estrogen and progesterone increases significantly and substantially within three years of beginning hormone use. The data showed no increased risk for women who used estrogen and progesterone for less than two years, potentially identifying a "safe" period for estrogen and progesterone use.---The study also found no increased risk of breast cancer in women who had stopped using estrogen and progesterone two or more years ago, suggesting a window of two to three years for the risks of estrogen and progesterone both to become apparent after initial use and to diminish after cessation. Few estimates of risk within two to three years of initiation and cessation are available, so these findings need replication in other large studies. The study found the use of estrogen and progesterone was associated with a doubling of risk of lobular cancer after three years of use, and a doubling of risk of ductal cancer with 10 years of use. Estrogen-only use was not associated with increased risk of ductal cancer, even after 20 years of use, but was associated with a 50 percent increase in risk of lobular cancer after 10 years of use.---Story Source: The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by American Cancer Society, via EurekAlert!, a service of AAAS. -- Journal Reference: --Eugenia E. Calle et al. ---Postmenopausal hormone use and breast cancer associations differ by hormone regimen and histologic subtype. Cancer, Published Online: January 20, 2008 DOI: 10.1002/cncr.24101

-----------------------------------------------------------------------------------------------

ScienceDaily (May 9, 2006) — Long-term estrogen therapy may be related to a higher risk of breast cancer among postmenopausal women who have had a hysterectomy, according to an article in the May 8 issue of Archives of Internal Medicine, one of the JAMA/Archives journals. ---Previous studies have linked the use of hormone therapy to breast cancer among postmenopausal women, but have primarily focused on the hormone combination of estrogen plus progestin, according to background information in the article. Recently released results from the Women's Health Initiative (WHI), a large clinical trial of hormone therapy, found no significant link between estrogen therapy and breast cancer in women who took the hormone for seven years. ---Wendy Y. Chen, M.D., M.P.H., Brigham and Women's Hospital and Dana Farber Cancer Institute, Boston, and colleagues evaluated women who were part of the Nurses' Health Study, a group of female nurses that have been followed since 1976. In 1980, 11,508 women from the study were postmenopausal and had had a hysterectomy. Every two years the researchers enrolled all the additional women who become postmenopausal and had a hysterectomy, so 28,835 women were included by the end of the study in 2002. Women were asked by questionnaire every two years if they used hormones and whether they had developed breast cancer. For women who developed breast cancer, the researchers obtained permission to review the women's medical records, which they used to record the hormone receptor information. Tumors were classified as positive or negative for estrogen receptor or progesterone receptor based on how they responded to specific hormonal therapies. ---Throughout the study period, 934 invasive breast cancers developed, 226 among women who had never used hormones and 708 among women who were using estrogen at the time. The longer a woman used estrogen, the higher her risk of breast cancer. Those who had been taking estrogen for fewer than 10 years did not appear to have a higher risk than those who had never taken hormones, but those who had been taking estrogen for more than 20 years had a significantly increased risk. The association was strongest for cancers that were estrogen receptor positive and progesterone receptor positive. The results were similar when the researchers evaluated only women who were older than age 60; only women who had begun estrogen therapy after reaching age 50; and only women who were at least age 50 and had undergone a hysterectomy, even if they had not gone through menopause. ---"In conclusion, we found that estrogen therapy was associated with an increased risk of breast cancer with longer-term use," the authors write. "Although current use of estrogen therapy for less than 10 years was not associated with a statistically significant increase in breast cancer risk, the WHI has shown an increased risk of stroke and deep-vein thrombosis in the same time period. Women who take estrogen therapy for prevention or treatment of osteoporosis typically require longer-term treatment and should thus explore other options, given the increased risk of breast cancer with longer-term use."---(Arch Intern Med. 2006; 166: 1027-1032. Available pre-embargo to media at www.jamamedia.org.) --Editor's Note: This study was supported by a grant from the National Institutes of Health, Bethesda, Md. ---Story Source: The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by JAMA and Archives Journals, via EurekAlert!, a service of AAAS ---

------------------------------------------------------------------------------------------------

ScienceDaily (Oct. 12, 2010) — Use of estrogen therapy is associated with an increased risk of developing kidney stones in postmenopausal women, according to a report in the October 11 issue of Archives of Internal Medicine, one of the JAMA/Archives journals.-- "Nephrolithiasis [kidney stones] is a common condition that affects 5 percent to 7 percent of postmenopausal women in the United States," according to background information in the article. "Because the process of kidney stone formation is influenced by a variety of lifestyle and other health-related factors, the true impact of estrogen therapy on the risk of kidney stone formation is difficult to infer from observational studies." -- Using data from the national Women's Health Initiative study, Naim M. Maalouf, M.D., of the University of Texas Southwestern Medical Center, Dallas, examined data from two trials: 10,739 postmenopausal women with hysterectomy who received either an estrogen-only treatment or matching placebo and 16,608 postmenopausal women without hysterectomy who received either an estrogen plus progestin treatment or matching placebo. Data were collected for an average of 7.1 years in the estrogen-only trial and 5.6 years for the estrogen plus progestin trial. -- A total of 335 cases of kidney stones were reported in the active treatment groups, while 284 cases occurred in the placebo groups. The beginning demographic characteristics and risk factors for kidney stones were similar in the two groups, and the authors found that estrogen therapy was associated with a significant increase in risk of kidney stones. The corresponding annualized incidence rate per 10,000 women per year was 39 in the treatment group and 34 in the placebo group. Development of kidney stones was five times more common in women with a history of kidney stones at the beginning of the study, but was not significantly altered by estrogen therapy. In this trial, estrogen therapy increased the risk of development of kidney stones irrespective of age, ethnicity, body mass index, prior hormone therapy use or use of coffee or thiazide diuretics.The authors conclude that their results "indicate that estrogen therapy increases the risk of nephrolithiasis in healthy postmenopausal women. The mechanisms underlying this higher propensity remain to be determined. In view of the sizable prevalence of nephrolithiasis in this segment of the population, these findings need to be considered in the decision-making process regarding postmenopausal estrogen use."---Story Source:--The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by JAMA and Archives Journals.--Journal Reference: N. M. Maalouf, A. H. Sato, B. J. Welch, B. V. Howard, B. B. Cochrane, K. Sakhaee, J. A. Robbins. Postmenopausal Hormone Use and the Risk of Nephrolithiasis: Results From the Women's Health Initiative Hormone Therapy Trials. Archives of Internal Medicine, 2010; 170 (18): 1678 DOI: 10.1001/archinternmed.2010.342

Fear of cancer prevents many women from restoring youthful hormone levels. When applied through the topical (transdermal) route, estriol is not associated with increased cancer risk. Other methods women can use to prevent hormone-related cancers include consuming abundant vitamin D, cruciferous vegetables, D-glucarate, and lignans, while minimizinghormone induced meat and high-fat BST dairy intake.—Interest in estriol increased as it was discovered that estriol was safer than horse-derived and synthetic hormones in relation to cardiovascular health and potentially cancer risk. Unfortunately, many doctors have not adopted its use, and many bioidentical hormone-replacement regimes use only estradiol, a more potent estrogen with increased associated risks.

RECIPE FOR ESTRIOL CONVERSION ---IODINE use Lugols iodine or a Iodoral or Nascent form at least once a day or consume foods that are high in Iodine such as sea weed or black walnut hull ( as a tea )Watercress-Irish moss-Iceland moss ( as a tea ice or hot ) as well as use a supplemental form of selenium or again consume foods that have good levels of selenium in them such as brazil nuts—garlic-onions-teas such as hawthorn, Bilberry, Astragalus, Sarsparilla

-----------------------------------------------------------------------------------------------

Using Nitroglycerin to Treat Prostate Cancer Shows Potential to Halt Disease

Red Wine Compound Shown To Prevent Prostate Cancer-- Recipe For Prostate Support

Prostate cancer hormone therapy may raise mortality

Silibinin inhibits established prostate tumor growth

ScienceDaily (Oct. 29, 2007) — Exercise may reduce, and even reverse, bone loss caused by hormone and radiation therapies used in the treatment of localized prostate cancer, thereby decreasing the potential risk of bone fractures and improving quality of life for these men, according to a new study. ---"Prostate cancer patients are not routinely advised to exercise. Walking is one tool that prostate cancer patients can use to improve their health and minimize the side effects of cancer and cancer treatments," said Paula Chiplis, PhD., RN, the lead author of the study and a clinical instructor and senior research assistant at Johns Hopkins Hospital in Baltimore. "Walking has no harmful side effects, if done moderately, but it can dramatically improve life for men suffering from side effects from some prostate cancer treatments." ---Men with localized prostate cancer frequently receive radiation therapy followed by months of hormone therapy to treat their cancer. Radiation is used to kill the cancer cells, while hormone therapy decreases testosterone and estrogen that feed the cancer cells, thereby keeping the tumor from growing. Men undergoing hormone therapy lose between 4 to 13 percent of their bone density on an annual basis, compared to healthy men who lose between .5 to 1 percent per year, beginning in middle age. Men are typically not thought to be at risk for osteoporosis and bone fractures; however, their rate of bone loss is greater than that of post-menopausal women. The study shows that prostate cancer patients undergoing hormone therapy that walked about five times a week for 30 minutes at a moderate pace maintained or gained bone density, while those who didn't exercise lost more than two percent of their bone density in eight to nine weeks. ---The study involved 70 sedentary men with Stage I-III prostate cancer, who were randomly assigned to either participate in the exercise plan or usual care (not exercise) during radiation treatment, with more than half also receiving hormone therapy. Researchers wanted to determine the effects of a nurse-directed, home-based walking program in maintaining physical function and managing cancer- and treatment-related symptoms during radiation and hormone treatment for prostate cancer patients.---This research "Effects of Exercise on Bone Loss & Functional Capacity during Prostate Cancer Treatment," was presented on October 28, 2007, at the American Society for Therapeutic Radiology and Oncology's 49th Annual Meeting in Los Angeles.---Story Source: The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by American Society for Therapeutic Radiology and Oncology, via EurekAlert!, a service of AAAS

----------------------------------------------------------------------------------------------

Using Nitroglycerin to Treat Prostate Cancer Shows Potential to Halt Disease

ScienceDaily (Feb. 11, 2010) — Treatment of prostate cancer using a very low dose of nitroglycerin may slow and even halt the progression of the disease without the severe side effects of current treatments, Queen's University researchers have discovered.--The findings are the result of the first-ever clinical trial using nitroglycerin to treat prostate cancer. The 24-month, Phase II study targeted 29 men with increasing levels of prostate-specific antigen (PSA) following prostate surgery or radiation. PSA levels are a key predictor of cancer progression.--"We were very excited to see a significant slowing in the progression of the disease as evidenced by the men's PSA levels, and to see this result in many of the men who completed the study," says Robert Siemens, the leader of the study and a Professor of Urology at Queen's University and urologist at Kingston General Hospital.--The researchers are encouraged by the results, particularly because safe and effective treatments for men with rising PSA levels following surgery or radiation are limited. They note that further testing needs to be done to confirm the results of this very small study.--The men were treated with a low-dose, slow-release nitroglycerin skin patch and their PSA levels monitored. Of the 17 patients who completed the study, all but one showed a stabilization or decrease in the rate of cancer progression, as measured by their PSA Doubling Time.---Nitroglycerin has been used at significantly higher doses for more than a century to treat angina. This trial was based on a key finding from pre-clinical research carried out at Queen's, which showed that decreases in nitric oxide play an important role in tumor progression and that this progression can be stopped by low-dose nitroglycerin.---Prostate cancer is diagnosed in approximately 235,000 men per year in the United States and 20,700 in Canada. Of patients who have undergone radical prostatectomy and/or radiation treatment, it is estimated that 30 to 50 percent will experience a recurrence of cancer. Results of the study, conducted by Queen's University researchers Robert Siemens, Jeremy Heaton, Michael Adams, Jun Kawakami and Charles Graham, appeared in a recent issue of the journal Urology.--Research into the use of nitroglycerin and similar compounds for the treatment of cancer by Drs. Adams, Graham and Heaton has resulted in the issue of 10 patents worldwide. PARTEQ Innovations, the technology transfer office of Queen's, has licensed some of this intellectual property to Nometics Inc., a Queen's spinoff company, which is developing products and therapies based on this and related research.--"This peer-reviewed research is our first clear clinical evidence that low-dose nitric oxide therapy offers prostate cancer patients a new non-invasive treatment option," says Robert Bender, CEO of Nometics. "It is our intention to start broader clinical trials in 2010 to confirm and expand these results."-Story Source: Adapted from materials provided by Queen's University

----------------------------------------------------------------------------------------------

Red Wine Compound Shown To Prevent Prostate Cancer-- Recipe For Prostate Support

ScienceDaily (Sep. 1, 2007) — Researchers at the University of Alabama at Birmingham (UAB) have found that nutrients in red wine may help reduce the risk of developing prostate cancer.The study involved male mice that were fed a plant compound found in red wine called resveratrol, which has shown anti-oxidant and anti-cancer properties. Other sources of resveratrol in the diet include grapes, raspberries, peanuts and blueberries. In the study resveratrol-fed mice showed an 87 percent reduction in their risk of developing prostate tumors that contained the worst kind of cancer-staging diagnosis. The mice that proved to have the highest cancer-protection effect earned it after seven months of consuming resveratrol in a powdered formula mixed with their food. Other mice in the study, those fed resveratrol but still developed a less-serious form of prostate cancer, were 48 percent more likely to have their tumor growth halted or slowed when compared to mice who did not consume the compound, the UAB research team said.This study adds to a growing body of evidence that resveratrol consumption through red wine has powerful chemoprevention properties, in addition to its apparent heart-health benefits, said lead study author Coral Lamartiniere, Ph.D., of UAB’s Department of Pharmacology and Toxicology.An earlier UAB study published May 2006 in the same journal found resveratrol-fed female mice had considerable reduction in their risk of breast cancer. Lamartiniere said his research team has been pleasantly surprised at the chemoprevention power of wine and berry polyphenols like resveratrol in animal models.“ A cancer prevention researcher lives for these days when they can make that kind of finding,” Lamartiniere said. “I drink a glass a day every evening because I’m concerned about prostate cancer. It runs in my family.” Lamartiniere and other researchers say work is already underway to test resveratrol consumption in humans to see what concentrations are needed to convey cancer-prevention benefits.--The amounts used in the UAB mice studies were the equivalent of one person consuming one bottle of red wine per day, which is not advisable. Since drinking alcohol in excessive amounts can have harmful health effects, doctors generally recommend moderate red wine consumption, which is an average of two drinks a day for men and one drink a day for women[U1].--Lamartiniere’s team included researchers from the UAB Department of Pathology and the Comprehensive Cancer Center. Funding support came from the U.S. Department of Defense and the National Cancer Institute.--The findings were published in August through the online edition of the Journal of Carcinogenesis.---Story Source:--Adapted from materials provided by University of Alabama at Birmingham.

Recipe For Prostate Support—One way to increase the potency is to fuse berries or grape extracts into a wine and repeatedly infusing this til there is a saturation and then allowing for some fermentation to take place –this will increase the effect of the antioxidant 0r you can buy the resveratrol and add it to a wine as well and then increasing the impact by using 1 ounce and then add 1 gram to this to get an increase this will suffice at a lower level of consumption---or take the resveratrol

------------------------------------------------------------------------------------------------

Prostate cancer hormone therapy may raise mortality

In elderly men with early-stage prostate cancer, receiving hormone therapy is associated with an increase in all-cause mortality, according to a study reported Tuesday at the American Society for Therapeutic Radiology and Oncology's 50th Annual Meeting underway in Boston. "Our study shows that for men over 70 with early-stage prostate cancer, androgen deprivation therapy as a form of treatment may do more harm than good," said Dr. Amy M. Dosoretz, a radiation oncology resident at the Harvard Radiation Oncology Program in Boston, who led the study. The findings of this study are "potentially practice-changing," said Dr. Louis Harrison of Beth Israel Medical Center, New York, and moderator of a press briefing where the findings were released. Dosoretz and colleagues reviewed the records of more than 1700 men, at least 70 years of age, with early-stage prostate cancer, who were treated with a short course of hormone therapy -- about 3.5 months -- before undergoing brachytherapy. Hormone therapy decreases levels of androgen, a hormone that stimulates the growth of prostate cancer cells. Brachytherapy is a procedure in which radiation "seeds" are strategically implanted in the prostate tumor that continuously release small doses of radiation to destroy the cancer cells. Some of the patients received brachytherapy alone. None of the men underwent conventional external-beam radiation therapy. After an average follow-up of 5.0 years, the men who received hormone therapy were 20 percent more likely to die from any cause compared with the men who received brachytherapy alone, Dosoretz reported. The findings were unchanged after the researchers adjusted the data to include the patient's age and factors known to influence the prognosis of prostate cancer. It's currently unclear why hormone therapy before radiation seed implantation would increase the risk of death in older men with early-stage prostate cancer, Dosoretz said. However, the presence of other illnesses could raise the risk of treatment-related complications, including cardiovascular complications, she suggested. "Our message is that in older patients it is very important to weigh the risks and benefits of hormone therapy when designing a treatment plan," Dosoretz told conference participants

---------------------------------------------------------------------------------------------

Silibinin inhibits established prostate tumor growth, progression, invasion, and metastasis and suppresses tumor angiogenesis and epithelial-mesenchymal transition in transgenic adenocarcinoma of the mouse prostate model mice

Authors' Affiliations: Department of Pharmaceutical Sciences, School of Pharmacy.

PURPOSE: The chronic nature of prostate cancer growth and progression leading to metastasis provides a large window for intervention. Herein, for the first time, we investigated the effect and associated mechanisms of silibinin phosphatidylcholine (silybin-phytosome) on established prostate tumors in transgenic adenocarcinoma of the mouse prostate (TRAMP) model. EXPERIMENTAL DESIGN: Twenty-week-old TRAMP male mice having palpable prostate tumor were fed with control or 0.5% and 1%, w/w, silybin-phytosome diets for 11 weeks and then sacrificed. RESULTS: Dietary silibinin inhibited the growth of prostate tumors (up to 60%, P < 0.001) and suppressed tumor progression from prostatic intraepithelial neoplasia to differentiated adenocarcinoma and poorly differentiated adenocarcinoma, with a complete absence of poorly differentiated adenocarcinoma at higher doses. It also inhibited the incidence of tumor invasion of seminal vesicle (up to 81%, P < 0.001) with complete absence of distant metastasis. Silibinin moderately inhibited tumor cell proliferation and induced apoptosis, but strongly suppressed tumor microvessel density (up to 60%, P < 0.001), vascular endothelial growth factor, and vascular endothelial growth factor receptor-2 expression. Antibody array analysis of plasma showed a decrease in the circulatory levels of vascular endothelial growth factor and basic fibroblast growth factor. Decreased levels of matrix metalloproteinases (MMP), snail-1, and vimentin, and an increased level of E-cadherin were also observed, indicating the anti-epithelial-mesenchymal transition effect of silibinin in tumors. CONCLUSIONS: Overall, silibinin treatment of TRAMP mice bearing prostate tumor inhibited tumor growth, progression, local invasion, and distant metastasis involving suppression of tumor angiogenesis and epithelial-mesenchymal transition. These findings would have greater relevance for the ongoing phase II clinical trial with silibinin-phytosome in prostate cancer patients.

--------------------------------------------------------------------------------------------------------------------------------

-----------------------------------------------------------------------------------------------------------------------------------------------------------------------------------

Combine ingredients in a Mason Jar (2qt, half the ingredients for a 1qt mason jar of course) Use all dried and chopped ingredients. 4tbsp Rosemary 4tbsp Sage
4tbsp Lavender 4tbsp Wormwood 4tbsp Peppermint 2 Quarts Braggs Organic Apple Cider Vinegar (With Mother) Combine all of these ingredients in the jar, shake them up vigorously for at least 2-3 minutes then place in your refrigerator. This must stay in the refrigerator for at last 2 weeks, and you should shake the mixture for at least 1 minute each day. At the end of 2 weeks chop up enough fresh garlic to make 4 tablespoons and add this to the mixture. Store in the refrigerator for another 1-2 weeks, shaking each day as needed. At the end of the 4 weeks strain out any chunks/particles from the mixture to the point it is fine enough to spray in a spray bottle. I grade down my straining from a screen, tea strainer, and finally a coffee filter. In terms of the herbs, I recommend only fresh dried and ground up varieties, it is very cheap, and a single pound will be enough for many many years of

It seems England is joining Germany in the 'war' against obese children. Parents who fail to help an obese child eat and exercise properly, ignoring all advice and guidance, could be guilty of neglect, child health experts say today.[U1] Doctor Russell Viner and colleagues from the UCL Institute of Child Health in London say that the weight of a child by itself is not a reason for child protection staff to get involved. But in an article on what they accept is a potentially contentious issue, published online today by the British Medical Journal, they suggest that it may be appropriate to consider the child protection register if the parents consistently fail to change the family's lifestyle and will not engage with outside help. "Parental failure to provide their children with adequate treatment for a chronic illness (asthma, diabetes, epilepsy, etc) is a well accepted reason for a child protection registration for neglect," they write.---Removing children from their parents may not help obesity. There are few data on the weight of children in public care," they say. A recent study found that 37% of children in care were overweight or obese - but almost all of them had put on weight after they were put into care.[U2] Yet another example of government pointing the finger at parents. Parents don't have the millions of dollars to gain political power. The corrupt food production and personal care companies run rampant with toxic ingredients while parents are overwhelmed with which products to chose for their families. I'm sure Big Pharma will be standing at the trough to pump 'special' drugs into these imprisoned children. What's next? ADHD kids will be imprisoned? Obese couples cannot have children? Even worse is data EXISTS for children who have been snatched. Truly disgusting action by wayward governments! How about starting with obese government policy makers!

Genetically Modified Salmon Must Be Labelled
FDA’s proposal to label GM salmon for production outside the US is
unenforceable, and its failure to extend labelling in the market borders on public deception[U3] Prof. Joe Cummins -This report has been submitted to the US FDA, please forward and circulate as widely as possible The Food and Drug Administration (FDA) held a public hearing regarding the labelling of food derived from AquAdvantage’s genetically modified (GM) Atlantic salmon. The purpose of the hearing was for FDA to explain the relevant legal principles for food labelling and to solicit information and views from the public. In a separate but related process, FDA held a public Veterinary Medicine Advisory Committee (VMAC) meeting and sought public input on safety and environmental impact of AquAdvantage salmon [1]. VMAC met on 19-20 September 2010, and considered comments including the advice that commercial release of AquaAdvantage salmon is too hazardous to consider in the absence of animal feeding studies [2] (AquaAdvantage Salmon Ready for Commerce? SiS 48). The VMAC committee failed to come to agreement, leaving the important issues undecided. The FDA discussion on labelling of the AquAdvantage salmon was convened on 21 Sept, but the input of comment was extended until 22 November 2010.

Labelling issues --The labelling issues considered by FDA include the following: 1. Which facts about the AquAdvantage salmon seem most pertinent for FDA’s consideration of whether there are any “material” differences between foods from this salmon and foods from other Atlantic salmon. (Keep in mind that the use of genetic engineering does not, in and of itself, constitute a ‘‘material’’ difference under the law.)[U4]

2. If FDA determined there are “material” differences”, how would that
difference be described on a food labelling in a way that is truthful and not
misleading. (Keep in mind that it is the difference in composition, or in
functional, organoleptic (odour, taste or texture) or other material properties
that must be described, not the underlying production process.) Information
about changes in the attributes of the food itself, such as its nutritional
value, functional properties (e.g., storage) or organoleptic qualities may be
important. --When commenting on these issues, FDA requests that respondents include support for their answers with relevant data, where appropriate, and/or references to the relevant legal principles. --FDA requires labelling of GM salmon but is uncertain about GM salmon in market--In the VMAC briefing packet [3], Section 3.4 of the Environment Assessment presents information on labelling of the product, including several warning
statements expected to appear on the product label: “fish must be reared in
land-based, highly contained systems that prevent their release into the environment” and the “fish cannot be reared in conventional cages or net pens deployed in open bodies of water.” Presumably this may mean that the GM salmon will be labelled prior to marketing for sale as food, at which time, the labels will be removed to conceal the GM origins of the salmon to be sold as food. The introduction of transgenes and their products into the GM salmon is not considered to be a material change in Atlantic salmon even though such changes would never have appeared in natural Atlantic salmon throughout its evolutionary history.

J Pharm Biomed Anal. 2010 Oct 10;53(2):137-44--Authors: Millet A, Stintzing F, Merfort I

An HPLC method, which allows reliable quantitation of flavonols and other phenolics in birch leaf extracts, was developed and validated. The method was applied to study the bioconversion of flavonols in fermented aqueous extracts. Almost 100% of the flavonols were converted during the 12 months observation period. The generated phenolics as well as consecutive conversion products were identified by HPLC-DAD, LC-MS and GC-MS techniques.---PMID: 20189738 [PubMed - indexed for MEDLINE]* Interesting concept here by taking in the leaves of the birch tree you can ferment the leave s and after a year would have a pretty potent pain killer as well as a immune enhancer and potentially cnacer and viral killer

CHICAGO (Reuters) - The U.S. Food and Drug Administration is cracking down on the over-the-counter sale of so-called chelation products that claim to treat conditions such as autism, heart disease and Alzheimer's by removing heavy metals from the body.---The FDA said on Thursday it sent warning letters to eight companies telling them their products were unapproved drugs and devices, and any claims about treating medical conditions with these products violated federal law.--"These products are dangerously misleading because they are targeted to patients with serious conditions and limited treatment options," Deborah Autor, director of the Office of Compliance in the FDA's Center for Drug Evaluation and Research, said in a statement.--"The FDA must take a firm stand against companies who prey on the vulnerability of patients seeking hope and relief[U5]," Autor said.---Although there are FDA-approved chelation drugs that are used in cases of heavy metal poisoning with a prescription, no chelation therapy products are approved for sale over the counter or on the Internet, the FDA said.---"What we're telling consumers today is that any chelation therapy marketed over the counter is suspect," Michael Levy, director of the FDA's Division of New Drugs and Labeling Compliance, told a telephone briefing.--Serious safety issues have been linked with chelation products, which can alter the levels of certain substances in the blood.[U6] Even when used under medical supervision, these products can cause serious harm, including dehydration, kidney failure and death.--One child died while being treated for autism with an intravenous chelation product[U7], FDA officials told the briefing. And they said there are likely many cases of serious side effects because companies are not compelled to report adverse events to the agency.--Companies that got the warning letters claim that their products treat a range of diseases by removing toxic metals from the body, the agency said.---Some also claim to treat autism spectrum disorder, cardiovascular diseases, Parkinson's disease, Alzheimer's disease, macular degeneration -- a major cause of blindness -- and other serious conditions, the FDA said.--And some companies that got warning letters also make test kits and claim their products can detect heavy metals, thereby justifying the need for chelation therapy.The FDA issued the warning because agency officials said there has been an increase in claims for and the availability of these products sold directly to consumers[U8].---The FDA said companies need to act quickly to correct violations listed in the warning letters or face possible legal action, including seizure of their products.--The letters were issued to the following companies: World Health Products LLC; Hormonal Health LLC; Evenbetternow LLC; Maxam Nutraceutics/Maxam Laboratories; Cardio Renew Inc; Artery Health Institute LLC; Longevity Plus, and Dr. Rhonda Henry, a nutritionist.áSupport them!!!—My personal comment is to supprot these companies

--------------------------------------------------------------------------------------------

[U1]Another Excuse For the State to take over your Children and regulate them and to teach them "There Way" and to violate anything that they do not see fit or that will compete for ther authority, alot of innuendo here to give off the idea that the state really cares for your offspring, But in reality they need slaves to do there bidding---If they really wanted to stop any obesity they would outlaw Mcdonalds and any other fast food franchise and eliminate all box foods that would disrupt the endocrin and digestive system and immune functions--instead these companies are allowed to sell " Posioned Foods " that shut down the brain or overload the brain so then there is an overwhelming compulsion to consume sugary foods which contribute to obesity

[U2]SO if this is tehe case then the Gov't would be libel for neglect and can be sued!!!!!!---and Should be---if the parents are feeding things to kids that are causing this issue and then the gov't follows suit with the same type of foods under "There Guidelines" which by the way are off---then the gov't would be involved in acting in the same irresponsible behaviour and as a result should be sued and there power base removed from any interference in matters such as these

[U3]Interesting thought here eh!! you label a GMO Fish Outside of the USA border ( Canada as well ) and what happens---these fish wind up in a streeam or ocean where they mate--then what happens--you have the GE gene now being transferred into the wild life-making these fish the sole propriety owner ship of the Corporates who came up with this technolgy-and ten ther eis the eco system that they are now contaminating with these genes--the ocean is alot more difficult to monitor then the land( and even that is not done efficiently, Look at our Bee's and this is just one species ---no one has looked at the ant or the earthworm or if they have they have not revelaed anything as of yet

[U4]Again this is such an oxymoron here that it is not considered a material difference under the law---Now anyone can see this is a farse at best there are laws but then there is science and in this--there would be a huge division in that anytime you are tampering with the genome( genetics) of anything there will be a change and potential anomalies that would not otherwise be present---this is to appease the people who would make a distinction or rebel to appease the resistance but nonetheless this does not change the fact that these fish are genetically altered and will cause a genetic disturbance in people as well as other fish---Look at Soy and canola--these 2 GE foods have caused all kinds of genetic anomalies in people and the land---the fish which would be more transient would spread the genetics across the oceans

[U5]The wording as per usual is always misleading and double talk---let's translate this in real earth language--we do not want you to have access too theses products because they will undermine our plan for eugenics---these products will pull out of the body all the chemtrail and exhaust fumes people are exposed to daily and will remove from the system the mercury in foods such as fish oils ) and other contaminats which we are unable to monitor but can indeed kill

[U6]WHAT stupidity--anything you consume can do this--alter the blood--What I find incredible is SOY

[U7]this again is Funny and sad that they are using this kind of scare mongering---if this actually happened at all it would have been done in the privacy of a doctors office or a Naturapth and I am not sure this would have been what killed

[U8]NOWWW Finallly the truth ---these companies are making more money then the counterpart in the pharmaceutical side

-------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------

-------------------------------------------------------------------------------------------------------------------

⁴ Division of Nutritional Sciences, University of Illinois, Urbana, IL 61801; ⁵ Integrative Immunology and Behavior Program, University of Illinois, Urbana, IL 61801; ⁶ Department of Animal Sciences, University of Illinois, Urbana, IL 61801

A dysregulated overexpression of inflammatory mediators by microgliamay facilitate cognitive aging and neurodegeneration. Considerableevidence suggests the flavonoid luteolin has antiinflammatoryeffects, but its ability to inhibit microglia, reduce inflammatorymediators, and improve hippocampal-dependent learning and memoryin aged mice is unknown. In initial studies, pretreatment ofBV-2 microglia with luteolin inhibited the induction of inflammatorygenes and the release of inflammatory mediators after lipopolysaccharide(LPS) stimulation. Supernatants from LPS-stimulated microgliacaused discernible death in Neuro.2a cells. However, treatingmicroglia with luteolin prior to LPS reduced neuronal cell deathcaused by conditioned supernatants, indicating luteolin wasneuroprotective. In subsequent studies, adult (3–6 mo)and aged (22–24 mo) mice were fed control or luteolin(20 mg/d)-supplemented diet for 4 wk and spatial working memorywas assessed as were several inflammatory markers in the hippocampus.Aged mice fed control diet exhibited deficits in spatial workingmemory and expression of inflammatory markers in the hippocampusindicative of increased microglial cell activity. Luteolin consumptionimproved spatial working memory and restored expression of inflammatorymarkers in the hippocampus compared with that of young adults.Luteolin did not affect either spatial working memory or inflammatorymarkers in young adults. Taken together, the current findingssuggest dietary luteolin enhanced spatial working memory bymitigating microglial-associated inflammation in the hippocampus.Therefore, luteolin consumption may be beneficial in preventingor treating conditions involving increased microglial cell activityand inflammation.^\

^{=----------------------------------------------------------------------------------------------------------------------------------------------}

Luteolin inhibits LPS-stimulated inducible nitric oxide synthase expression in BV-2 microglial cells.

Abstract

Overproduction of nitric oxide (NO) by inducible nitric oxide synthase (iNOS) acts as a neurotoxic effector in the central nervous system, resulting in neurodegenerative diseases. From the alcoholic extracts of Perilla frutescens, we have purified an inhibitor of NO production in lipopolysaccharide (LPS)-activated microglia by activity-guided purification. The active compound was identified as luteolin by spectral analysis. Luteolin inhibited the NO production in LPS-activated microglia in a dose-dependent manner (IC50=6.9 microM). Luteolin also suppressed the degradation of I-kappaB-alpha, the expression of protein and mRNA of iNOS in LPS-activated microglia as observed in Western blot analysis and RT-PCR experiments. Luteolin may have beneficial effects in the treatment of neuro-inflammatory diseases through the inhibition of iNOS expression

----------------------------------------------------------------------------------------

Manuscript received 15 April 1998. Initial reviews completed 13 May 1998. Revision accepted 4 August 1998.

Hashim E. Osman, Nabil Maalej, Dhanansayan Shanmuganayagam, and John D. Folts

Platelet aggregation (PA) contributes to both the development of atherosclerosis and acute platelet thrombus formation (APTF)followed by embolization producing cyclic flow reductions (CFR) in stenosed and damaged dog and human coronary arteries. In seven anesthetized dogs with coronary stenosis and medial damage, CFR occurred at 7 ± 3/30 min and were abolished 127 ± 18 min after gastric administration of 10 mL of purple grape juice/kg. Collagen-inducedex vivo whole blood PA decreased by 49 ± 9% after the abolishmentof CFR with grape juice. Ten mL of orange juice/kg (n = 5) and10 mLof grapefruit juice/kg (n = 5) had no significant effecton the frequency of the CFR or on ex vivo PA. In vitro studies have suggested that flavonoids bind to platelet cell membranesand thus may have an accumulative or tissue-loading effect overtime. To test this we fed 5 mLof grape juice/kg to 5 cynomologousmonkeys for 7 d. Collagen-induced ex vivo PA decreased by 41 ±17% compared to control (pre-reatment) after 7 d of feeding. Inthe same 5 monkeys, neither 5 mL of orange juice/kg nor 5 mLofgrapefruit juice/kg given orally for 7 d produced any significantchange in PA. Grape juice contains the flavonoids quercetin, kaempferoland myricetin, which are known inhibitors of PA in vitro. Orangejuice and grapefruit juice, while containing less quercetin thangrape juice, primarily contain the flavonoids naringin, luteolinand apigenin glucoside. The flavonoids in grapes were shown invitro to be good inhibitors of PA, whereas the flavonoids in orangesand grapefruit to be poor inhibitors of PA. The consumption ofgrape juice, containing these inhibitors of PA, may have someof the protection offered by red wine against the developmentof coronary artery disease (CAD) and acute occlusive thrombosis,whereas orange juice or grapefruit juice may be ineffective. Thus,grape juice may be a useful alternative dietary supplement to red wine without the concomitant alcohol intake.

^{---------------------------------------------------------------------------------------------------------------------------------------------}

Grape juice, but not orange juice or grapefruit juice, inhibits human platelet aggregation.

Cardiology Section of Department of Medicine, University of Wisconsin, Madison, WI 53792, USA.

Abstract

Coronary artery disease is responsible for much mortality and morbidity around the world. Platelets are involved in atherosclerotic disease development and the reduction of platelet activity by medications reduces the incidence and severity of disease. Red wine and grapes contain polyphenolic compounds, including flavonoids, which can reduce platelet aggregation and have been associated with lower rates of cardiovascular disease. Citrus fruits contain different classes of polyphenolics that may not share the same properties. This study evaluated whether commercial grape, orange and grapefruit juices, taken daily, reduce ex vivo platelet activity. In a randomized cross-over design, ten healthy human subjects (ages 26-58 y, five of each gender) drank 5-7.5 mL/(kg. d) of purple grape juice, orange juice or grapefruit juice for 7-10 d each. Platelet aggregation (whole blood impedance aggregometry, Chronolog Model #590) at baseline was compared to results after consumption of each juice. Drinking purple grape juice for one week reduced the whole blood platelet aggregation response to 1 mg/L of collagen by 77% (from 17.9 +/- 2.3 to 4.0 +/- 6.8 ohms, P = 0.0002). Orange juice and grapefruit juice had no effect on platelet aggregation. The purple grape juice had approximately three times the total polyphenolic concentration of the citrus juices and was a potent platelet inhibitor in healthy subjects while the citrus juices showed no effect. The platelet inhibitory effect of the flavonoids in grape juice may decrease the risk of coronary thrombosis and myocardial infarction.

-------------------------------------------------------------------------------------------

Remedy with Grape Juice Concentrate---to get a good dose of this effect Go to the Wine shops where you can buy real grape concentrates with out all the sugar then you can dilute it to your level and consume this---if you cannot consume wine this maybe the next thing that maybe an alternative to you—to increase the luteolin effect add dandelion—parsley-rosemary –to the grape concentrate and blend til smooth—or for at the least 10 min high speed or til blender container feels hot—pour the fused contents into a Glass Container –date and mark and use 1 ounce several times a day---

---------------------------------------------------------------------------------------------

Salvia officinalis L.: composition and antioxidant-related activities of a crude extract and selected sub-fractions.

Faculty of Pharmacy, Department of Pharmaceutical Biology, University ofHelsinki, POB 56 (Viikinkaari 5E), FIN-00014, Finland.

Abstract

The composition and antioxidant properties of a methanol: acetic acid (99:1, v/v) soluble crude extract isolated from S. officinalis L. leaves through maceration and selected fractions isolated thereof are presented in this study. The total phenol content was estimated as gallic acid equivalents, whilst qualitative-quantitative phenolic content was determined using high performance liquid chromatography with photodiode array detection. Antioxidant evaluation consisted of ferric reductive capacity and 1,1-diphenyl-2-picrylhydrazyl and hydroxyl free radical scavenging determinations. The crude extract contained hydroxybenzoic acids, hydroxycinnamic acids, flavonoids and diterpenoids, whilst caffeic acid, carnosic acid, luteolin, luteolin-7-O-glucoside and rosmarinic acid were identified from their chromatographic and spectral characteristics and quantified from their respective calibration curves. The crude extract and sub-fractions demonstrated varying degrees of efficacy in the antioxidant-related assays used, except the n-hexane fraction, which was unable to reduce iron(III) at reasonable concentrations. Although the positive controls, ascorbic acid, BHA and BHT, were more potent than the S. officinalis samples, two fractions were significantly (p < 0.05) more potent iron(III) reducing agents than pycnogenol, a proanthocyanidin-rich commercial preparation

----------------------------------------------------------------------------------------------

Flavonoids and phenolic compounds from Rosmarinus officinalis.

Abstract

A new flavonoid, 6''-O-(E)-feruloylhomoplantaginin (1), and 14 known compounds, 6''-O-(E)-feruloylnepitrin (2), 6''-O-(E)-p-coumaroylnepitrin (3), 6-methoxyluteolin 7-glucopyranoside (4), luteolin 3'-O-beta-D-glucuronide (5), luteolin 3'-O-(3''-O-acetyl)-beta-D-glucuronide (6), kaempferol (7), luteolin (8), genkwanin (9), and ladanein (10), together with 1-O-feruloyl-beta-D-glucopyranose (11), 1-O-(4-hydroxybenzoyl)-beta-D-glucopyranose (12), rosmarinic acid (13), carnosic acid (14), and carnosol (15), were isolated from the leaves of Rosmarinus officinalis . The structures were established on the basis of NMR spectroscopic methods supported by HRMS. All isolated compounds were tested for cytotoxicity in human cancer cell lines (HepG2, COLO 205, and HL-60) and for anti-inflammatory activities in lipopolysaccharide (LPS)-treated RAW 264.7 macrophage cells. Among them, compounds 14 and 15 were modestly active in the inhibition of nitrite production in macrophages, followed by compounds 8 and 5. Compounds 14 and 15 were more effective as an antiproliferative agent in HL-60 cells with IC(50) values of 1.7 and 5.5 microM, followed by compounds 8 and 7 with IC(50) of 39.6 and 82.0 microM, respectively. In addition, compounds 14 and 15 showed potent antiproliferative effects on COLO 205 cells with IC(50) values of 32.8 and 29.9 microM, respectively.

----------------------------------------------------------------------------------------

Distribution and biological activities of the flavonoid luteolin.

Department of Pharmacology, Faculty of Pharmacy, University of Seville, Spain. C/ Profesor Garcia Gonzalez, 41011, Sevilla, Spain. mlopezlazaro@us.es

Abstract

Epidemiological evidence suggests that flavonoids may play an important role in the decreased risk of chronic diseases associated with a diet rich in plant-derived foods. Flavonoids are also common constituents of plants used in traditional medicine to treat a wide range of diseases. The purpose of this article is to summarize the distribution and biological activities of one of the most common flavonoids: luteolin. This flavonoid and its glycosides are widely distributed in the plant kingdom; they are present in many plant families and have been identified in Bryophyta, Pteridophyta, Pinophyta and Magnoliophyta. Dietary sources of luteolin include, for instance, carrots, peppers, celery, olive oil, peppermint, thyme, rosemary and oregano. Preclinical studies have shown that this flavone possesses a variety of pharmacological activities, including antioxidant, anti-inflammatory, antimicrobial and anticancer activities. The ability of luteolin to inhibit angiogenesis, to induce apoptosis, to prevent carcinogenesis in animal models, to reduce tumor growth in vivo and to sensitize tumor cells to the cytotoxic effects of some anticancer drugs suggests that this flavonoid has cancer chemopreventive and chemotherapeutic potential. Modulation of ROS levels, inhibition of topoisomerases I and II, reduction of NF-kappaB and AP-1 activity, stabilization of p53, and inhibition of PI3K, STAT3, IGF1R and HER2 are possible mechanisms involved in the biological activities of luteolin.

--------------------------------------------------------------------------------------------

Special Note---Go to www.youtube.com and then type in herbsplusbeadworks in the search box and see how to make a green drink Extract with parsley dandelion and watercress these all have luteolin and apigenenin in them as well as other antioxidants and nutrients--This is a small investment and can be easily grown in a garden or a pot or crate or any means you have to et it going

---------------------------------------------------------------------------------------------------------------------------------------------------------------------

Natural Alpha Tocopherol (Vitamin E) in the treatment of Cardiovascular and Renal Diseases as suggested by Drs. Wilfrid and Evan Shute and the Shute Institute for Clinical and Laboratory Medicine, London, Ontario, Canada. Use only products labeled in terms of InternatIonal Units (IU).

Acute coronary thrombosis: 450 to 1,600 IU a day started as soon as possible and maintained.

Older cases of coronary thrombosis: 450 to 1,600 IU if systolic pressure is under 160 Otherwise 450 IU for the first four weeks, particularly if a hypotensive agent is used concurrently.

Chronic rheumatic heart disease: give 90 IU daily first month, 120 IU daily second month and 150 IU daily for third month. 150 IU may be ideal dose. Occasionally more is necessary and advisable. Response will necessarily be slow.

Anginal Syndrome: 450 to 1,600 IU if systolic pressure is under 160. Otherwise start on 150 IU for four weeks then 300 IU for four weeks, particularly if hypotensive agent is used.

Hypertensive heart disease: 75 IU daily for four weeks, 150 IU daily for four weeks, then cautiously increase. Should be used with hypotensive agents. High doses of vitamin E have been shown to reduce high blood pressure in rats with chronic kidney failure. (Vaziri N. Hypertension, Jan 2002.)

Burns, Plastic Surgery, Mazoplasia: 600 to 1,600 IU daily, using vitamin E ointment or vitamin E spray as adjunct. (Editor’s note: vitamin E may also be dripped from a thumbtack-punctured capsule.)

Do not take iron and vitamin E at same time. If iron is indicated, separate the doses by about nine hours. -The digitalis requirement is often reduced after vitamin E takes hold, so over-digitalization should be avoided. A patient receiving vitamin E should not be digitalized by the Eggleston massive dose technique nor any of its modifications. It is usually sufficient for full digitalization to give what is ordinarily a maintenance dose of 1 1/2 grains digitalis folia or 0.1 mg digitoxin per day. By the second day the patient is often digitalized.

Insulin dosages in diabetic cardiacs must be watched closely, for the insulin requirement may be considerably reduced very suddenly. -Hyperthyroidism is sometimes a contraindication.

Estrogens should rarely be given at the same time as alpha tocopherol (vitamin E).

(Editor's note: The Shutes also recommend caution with patients who have untreated high blood pressure, a rheumatic heart, or congestive heart failure. If you are a person with these or any other preexisting medical condition, you need to WORK WITH YOUR PHYSICIAN TO DETERMINE YOUR OPTIMUM VITAMIN E LEVEL.)

1. It reduces the oxygen requirement of tissues.
Hove, Hickman, and Harris (1945) Arch. Biochem. 8:395.

Telford et al (1954) Air University School of Aviation Medicine Project #21-1201-0013, Report #4, May. Randolph Field, Texas.

2. It melts fresh clots, and prevents embolism.
Shute, Vogelsang, Skelton and Shute (1948) Surg., Gyn. and Obst. 86:1.

3. It improves collateral circulation.
Enria and Fererro (1951) Arch. per Ia Scienze Med. 91:23.

4. It is a vasodilator.
Shute, Vogelsang, Skelton and Shute (1948) Surg., Gyn. and Obst. 86:1.

5. It occasionally lyses scar tissue.
Steinberg (1948) Med. Clin. N. America 30:221, 1946.

6. It prevents scar contraction as wounds heal.
Shute, Vogelsang, Skelton and Shute (1948) Surg., Gyn. and Obst. 86:1.

7. It increases low platelet counts.
SkeIton, Shute, Skinner and Waud (1946) Science 103:762.

8. It decreases the insulin requirement in about 1/4 of diabetics.
Butturini (1950) Gior. di Clin. Med. 31:1.

9. It is one of the regulators of fat and protein metabolism.
Hickman (1948) Rec. of Chem. Progress, p.104.

11. It preserves capillary walls.
Ames, Baxter and Griffith (1951) International Review of Vitamin Research 22:401.

12. It prevents haemolysis of red blood cells.
Rose and Gyorgy (1951) Fed. Proc.10:239. 1951.

Tolgyes, S. and Shute, E. V. (1957), Alpha Tocopherol in the Management of Small Areas of Gangrene. Can. M. A. J. 76:730.

Shute, E.V. (1957) The Prevention of Congenital Anomalies in the Human: Experiences with Alpha Tocopherol as a Prophylactic Measure. J. Ob. & Gyn. Brit. Emp. 44:390.

Hauch, J. T. (1957) A New Treatment for Resistant Pressure Sores. Can. M.A.J. 77:125.

Shute, E. V. (1957) Alpha Tocopherol in Cardiovascular Disease. Oxford University Med. Gaz. 9:96.

Scramble your eggs in a bowl. Pour them in a saute pan and cook until done. ( an alternative would be to hard boil the eggs as well and then peel off the shell and place in bowl and mash the eggs down till the eggs are in a crumbly or crushed condition)--- Drain the excess grease for a few minutes on a paper towel. Break the eggs into tiny pieces.--Spread the eggs out onto a baking sheet. Dry at 135° F for at least 10 hours.--Run the eggs through a blender until they form a fine powder. Store your powdered eggs either in a glass container or a jar with a tight lid.---you may need to add some salt as a preservative---- How to Make Powdered Eggs http://www.ehow.com/how_2304324_make-powdered-eggs.html#ixzz130Srsk3S

--------------------------------------------------------------------------------------------

USE VERY FRESH EGGS ONLY.
The yolks should be firm and the whites thick. Fresh eggs will sink when placed in cold water.

SEPARATE EGG WHITES AND YOLKS.
Beat egg whites into a stiff meringue. Spread on a Teflon tray.
Beat egg yolks until thick and foamy. Pour on to a separate pyrex or a nonstick material. ( some may use Teflon since it is non stick—that will be for you to determine

DRY BETWEEN 105° AND 115°.
Dry until crisp or brittle, usually about 10-12 hours.

POWDER DRIED EGG.
Crumble, then powder eggs using a dry food/seed grinder. Combine powdered yolks and whites. For a finer powder, re-dry for a few hours then grind once again.

áDrying Cooked Eggs: Peel hardboiled eggs and chop. Place in a pyrex or a nonstick material that is not hazardous. Yolks and whites may be dried separately or together. Dry at 105° to 115° for 8-10 hours.

Storing Dried Eggs:

Because of their fat content, dried eggs should be kept refrigerated. They should be kept only 3 or 4 weeks unless frozen. They will keep unrefrigerated for a week or so and are ideal for camping.—this is due to the fat if you hard boil them and then mash them down it will be with out the fats that may go rancid—and can be use stored with salt

Using Dried Eggs:

RAW EGGS:
Generally, 1-1/2 tablespoons of dried egg powders plus an equal amount of water is equivalent to one egg. This will vary slightly depending on the size of eggs you started with. When reconstituting dried COOKED EGGS, add slightly more than half as much water as egg.

Heavenly Scrambled Eggs

Mix together all ingredients. Let stand several minutes. Cook in oiled frying pan until done.
1 serving.

------------------------------------------------------------------------------------------------

I dehydrate eggs with a Mr. Coffee dehydrator. I do 6 at a time, and use the fruit roll sheet on the top tray. I beat the eggs as if I were going to make an omlette, then freeze them in a glass jar in the freezer overnight.---When I'm ready to dry them, I let them thaw, but not warm to room temp. Freezing seems to speed up the process a little. After about 18 hours of drying, they're dry and brittle. I powder them with an old coffee grinder, but a blender or food processor will work just as well. The egg powder goes into ziplock baggies, and in the cupboard.---I've used eggs that I've dehydrated this way for omlettes and cooking, with no problems. To rehydrate for use, I mix two measures of water for each measure of powder.---I have some eggs that were dehyrated over 5 years ago, and stored in the cupboard in a ziplock bag, that are still good to us---( Again Use some salt as a precaution to keep it preserved )—my special note

Tea polyphenols have been shown to have anticancer activity in many studies. In the present study, we investigated effects of theaflavin-3-3'-digallate (TF(3)), one of the major theaflavin monomers in black tea, in combination with ascorbic acid (AA), a reducing agent, and (-)-epigallocatechin-3-gallate (EGCG), the main polyphenol presented in green tea, in combination with AA on cellular viability and cell cycles of the human lung adenocarcinoma SPC-A-1 cells. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay showed that the 50% inhibition concentrations (IC(50)) of TF(3), EGCG, and AA on SPC-A-1 cells were 4.78, 4.90, and 30.62 micromol/L, respectively. The inhibitory rates of TF(3) combined with AA (TF(3)+AA) and EGCG combined with AA (EGCG+AA) at a molar ratio of 1:6 on SPC-A-1 cells were 54.4% and 45.5%, respectively. Flow cytometry analysis showed that TF(3)+AA and EGCG+AA obviously increased the cell population in the G(0)/G(1) phase of the SPC-A-1 cell cycle from 53.9% to 62.8% and 60.0%, respectively. TF(3)-treated cells exhibited 65.3% of the G(0)/G(1) phase at the concentration of its IC(50). Therefore, TF(3)+AA and EGCG+AA had synergistic inhibition effects on the proliferation of SPC-A-1 cells, and significantly held SPC-A-1 cells in G(0)/G(1) phase. The results suggest that the combination of TF(3) with AA or EGCG with AA enhances their anticancer activity.--PMID: 20506578 [PubMed - indexed for MEDLINE]

Bisphenol A officially declared toxic by Canada

Canada became the first country in the world yesterday to declare bisphenol A (BPA) to be a toxic substance that poses risks to human health and the environment. --The announcement by the Canadian Health and Environment Ministries confirmed the chemical had formally been added Schedule 1 of the Canadian Environmental Protection Act, 1999 (CEPA 1999). ---"The Government of Canada has a strong record of taking action on Bisphenol A to protect the environment and health of Canadians," said Environment Minister Jim Prentice. "We are continuing our leadership on this issue and...working hard to monitor and manage Bisphenol A." --BPA is an industrial chemical used to make a hard, clear plastic such as re-usable polycarbonate baby bottles. It is also used in the manufacture of epoxy resins, which act as a protective lining on the inside of metal-based food and beverage cans.

Danger to human life or health ---In the order adding BPA to the toxic register, Health Canada identified dietary intake as the primary source of human exposure. It underlined concerns regarding the link between the chemical and neurodevelopmental and behavioural effects in rodents and said it was “considered appropriate to apply a precautionary approach when characterizing risk to human health”. ---“Therefore, it was concluded that bisphenol A should be considered as a substance that may be entering the environment in a quantity or concentration or under conditions that constitute or may constitute a danger in Canada to human life or health,” said the government order.

Scientific opinions ---Canada’ s announcement yesterday is the culmination of two year’s deliberations and differs markedly from the recent opinion from the European Food Safety Authority (EFSA) which dismissed scientific concerns raised recently in scores of studies - including BPA's link with neurodevelopmental and behavioural effects. The European body said it had found no scientific evidence that would lead it to recommend altering the tolerable daily intake (TDI) of the chemical. ---The Canadian position decision on BPA was also reached in the face of fierce opposition from the chemical industry. The American Chemistry Council executive director Steven Hentges yesterday said the move was “contrary to the weight of worldwide scientific evidence, unwarranted and will unnecessarily confuse and alarm the public”. ---But the Canadian Government said its actions had been based on “robust and relevant scientific evidence”. It noted that Health Canada had considered both studies that were based on guidelines for good laboratory practice and those that were not because “they were considered relevant to risk characterization”. --"Our science indicated that Bisphenol A may be harmful to both human health and the environment and we were the first country to take bold action in the interest of Canadians,” said Leona Aglukkaq, Minister of Health.

ScienceDaily (Mar. 20, 2007) — When it comes to stocking pharmacy shelves with drugs to treat human ills, God’s Creation is still is the ultimate medicinal chemist, a study scheduled for the March 23 issue of ACS’ Journal of Natural Products, a monthly publication, suggests.

In the study, the National Cancer Institute’s David J. Newman and Gordon M. Craig conclude that only 30 percent of the critically important “new chemical entities (NCEs)” introduced between 1981 and mid-2006 were synthetic and not based on a naturally-occurring compound. NCEs are totally new drugs, never before available, rather than modified versions of existing medications sometimes termed “me-too” drugs. The remaining 70 percent of the NCEs introduced during the last 25 years were natural products — medicines obtained from sources such as plants and animals, derived from natural products or chemically designed to mimic natural products.--Natural products range from aspirin (originally obtained from the willow tree) to taxol, the anti-cancer drug discovered in the Pacific yew tree. About half of all anti-cancer drugs introduced since the 1940s are either natural products or medicines derived directly from natural products, the study notes.---The new review of natural products’ role as sources of new drugs is an expanded and updated version of reports published in 1997 and 2003. “We strongly advocate expanding, not decreasing, the exploration of Nature as a source of novel active ingredients that may serve as the leads and scaffolds for elaboration into desperately needed efficacious drugs for a multitude of disease indications,” the study concludes.--Story Source: -The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by American Chemical Society, via EurekAlert!, a service of AAAS

******************************************************************************************************

***************************************************************************************************************************

**************************************************************************************************

PURPOSE: US Dietary Guidelines recommend a daily sodium intake <2300 mg, but evidence linking sodium intake to mortality outcomes is scant and inconsistent. To assess the association of sodium intake with cardiovascular disease (CVD) and all-cause mortality and the potential impact of dietary sodium intake <2300 mg, we examined data from the Second National Health and Nutrition Examination Survey (NHANES II).

METHODS: Observational cohort study linking sodium, estimated by single 24-hour dietary recall and adjusted for calorie intake, in a community sample (n = 7154) representing 78.9 million non-institutionalized US adults (ages 30-74). Hazard ratios (HR) for CVD and all-cause mortality were calculated from multivariable adjusted Cox models accounting for the sampling design.

RESULTS: Over mean 13.7 (range: 0.5-16.8) years follow-up, there were 1343 deaths (541 CVD). Sodium (adjusted for calories) and sodium/calorie ratio as continuous variables had independent inverse associations with CVD mortality (P = .03 and P = .008, respectively). Adjusted HR of CVD mortality for sodium <2300 mg was 1.37 (95% confidence interval [CI]: 1.03-1.81, P = .033), and 1.28 (95% CI: 1.10-1.50, P = .003) for all-cause mortality. Alternate sodium thresholds from 1900-2700 mg gave similar results. Results were consistent in the majority of subgroups examined, but no such associations were observed for those <55 years old, non-whites, or the obese.

CONCLUSION: The inverse association of sodium to CVD mortality seen here raises questions regarding the likelihood of a survival advantage accompanying a lower sodium diet. These findings highlight the need for further study of the relation of dietary sodium to mortality outcomes.

------------------------------------------------------------------------------------------------

Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, New York 10461, USA. hicohen@aecom.yu.edu

Abstract

PURPOSE OF REVIEW: Persistent recommendations for universal restriction of dietary sodium intake are based on associations of sodium intake with blood pressure. No clinical trial data support an association of sodium intake with mortality and morbidity outcomes, however, while results of observational studies appear heterogeneous. Can these contradictory data be reconciled to inform health policy regarding sodium intake recommendations?

RECENT FINDINGS: We reported (2006) a statistically significant (P = 0.03) association of sodium intake less than 2.3 g/day with increased cardiovascular disease mortality (hazard ratio 1.37) in a representative sample of the US adult population with an observed baseline mean sodium intake of 2.7 g/day. Others reported (2004) a significant (P < 0.01) higher stroke death among males and borderline significant (P = 0.07) for females, for highest compared with lowest sodium tertile in a community in Japan with mean intake of 5.4 g/day.

SUMMARY: These results are consistent with earlier studies suggesting that the association of sodium with morbidity and mortality in industrial societies follows a 'J shape' with a direct association at high levels of average intake (over 4 g), an inverse association at lower levels (less than 2 g) and no measurable effect for the widely prevalent intakes in between.---PMID: 17556882 [PubMed - indexed for MEDLINE]

-----------------------------------------------------------------------------------------------

Perry IJ.--Department of Epidemiology and Public Health, University College Cork, Ireland.

Abstract

AIM: Diet is a major contributor to variation in the occurrence of hypertension and cardiovascular disease, including stroke, worldwide. Dietary salt intake plays a critical role in blood pressure regulation. However the question of whether high dietary salt intake increases risk of stroke, either indirectly via effects on blood pressure or directly via alternative mechanisms has received limited attention.

DATA SYNTHESIS: Narrative review of evidence linking dietary salt intake with left ventricular hypertrophy and cardiovascular disease end-points.

CONCLUSIONS: There is accumulating evidence that high salt intake predicts left ventricular hypertrophy, independent of other variables including body mass index and blood pressure. Data are now available from nine different studies worldwide consistent with a significant independent effect of salt intake on left ventricular hypertrophy. There is also evidence from animal experiments and ecological studies of an independent association between salt intake and risk of stroke. However, data from prospective observational studies on the relation between sodium intake and cardiovascular endpoints (including stroke) are sparse and inconsistent. Data from Alderman et al suggesting that there may be a significant inverse association between urinary sodium excretion and risk of cardiovascular disease has attracted controversy. In a number of prospective studies no association between salt intake and cardiovascular disease end-points (including stroke) has been observed. In a recent analysis from the US NHANES follow-up study, there was evidence that high salt intake is strongly and significantly associated with risk of stroke, other cardiovascular disease and all cause mortality in overweight persons, but not in those of normal weight. These findings need to be replicated. However, current data on the association between salt intake, blood pressure and left ventricular hypertrophy support public policy recommendations on the need for a moderate reduction in dietary salt intake at the population level.--PMID: 11079261 [PubMed - indexed for MEDLINE]

------------------------------------------------------------------------------------------

Diabetes and Genetic Epidemiology Unit, Department of Epidemiology and Health Promotion, National Public Health Institute, Mannerheimintie 166, FIN-00300 Helsinki, Finland. hu.gang@ktl.fi

Abstract

Dietary salt intake plays a major role in variation of blood pressure levels and cardiovascular conditions. High salt intake is associated with the occurrence of hypertension. The evidence that high salt intake increases risk of cardiovascular disease is inconsistent. Some studies indicate a significant and positive association between salt intake and risk of cardiovascular disease, whereas several other studies report that such an association may not exist and that low sodium may even be harmful. It is clear that left ventricular hypertrophy is closely related to salt intake. There is evidence indicating that high salt intake increases renal glomerular filtration rate and glomerular filtration fraction in salt-sensitive patients. The association of high salt intake, insulin resistance, and salt sensitivity, and the interaction between high salt intake, heart rate, and blood pressure are debated. ---PMID: 11790286 [PubMed indexed for MEDLINE]

------------------------------------------------------------------------------------------

Suggestions On Salt---if you are using salt and are uncertain of the negative impact -due to the programming we have been taught for a log time, then increase the potassium intake to balance this out--the ratio should be 2:1 --2 parts potassium and one part salt--as an example we would be using a half a tsp to 1 tsp of potassium here is another link to the page http://augmentinforce.50webs.com/The%20Need%20For%20SALT1.htm#SALT where you can increase the knowledge on the power of Salt--

Sodium Chloride alleviates Hyperchlorhydria (excessive Hydrochloric Acid):

People who crave Sodium (Salt) are often found to be suffering from Adrenal Insufficiency.

Cardiovascular System

Sodium increases the viscosity of Blood.
Sodium regulates osmotic Blood Pressure:
Sodium may alleviate Hypotension (by increasing Blood Pressure).
Sodium neutralizes Acidosis.
Sodium is a primary Electrolyte.

Digestive System

Sodium alleviates Constipation.
Sodium Sulfate alleviates Diarrhea.
Flatulence can occur as a result of Sodium deficiency.
Nausea can occur as a result of Sodium deficiency.
Vomiting can occur as a result of Sodium deficiency.

Excretory System

Optimal Sodium levels are required for the correct function of the Kidneys.

Eyes/Vision

Sodium deficiency can cause blurred vision in the Eyes.

Immune System

Sodium helps to reduce Fevers.
Optimal Sodium levels are required for the correct function of the Lymphatic System (Sodium is a component of Lymph).

TOP G